Abstract
A close association with its vertebrate and tick hosts allows Borrelia burgdorferi, the bacterium responsible for Lyme disease, to eliminate many metabolic pathways and instead scavenge key nutrients from the host. A lipid-defined culture medium was developed to demonstrate that exogenous lipids are an essential nutrient of B. burgdorferi, which can accumulate intact phospholipids from its environment to support growth. Antibody responses to host phospholipids were studied in mice and humans using an antiphospholipid ELISA. Several of these environmentally acquired phospholipids including phosphatidylserine and phosphatidic acid, as well as borrelial phosphatidylcholine, are the targets of antibodies that arose early in infection in the mouse model. Patients with acute infections demonstrated antibody responses to the same lipids. The elevation of antiphospholipid antibodies predicted early infection with better sensitivity than did the standardized 2-tier tests currently used in diagnosis. Sera obtained from patients with Lyme disease before and after antibiotic therapy showed declining antiphospholipid titers after treatment. Further study will be required to determine whether these antibodies have utility in early diagnosis of Lyme disease, tracking of the response to therapy, and diagnosis of reinfection, areas in which current standardized tests are inadequate.
Highlights
With an average genome of approximately 1.3 mbp [1], many aspects of cellular metabolism are minimized or absent in Borrelia burgdorferi
B. burgdorferi is unable to grow in a lipid-depleted growth medium, with growth being restored by supplementation with fatty acids and cholesterol (Figure 1A)
A standard Barbour-Stoenner-Kelly II (BSK) growth medium was stripped of lipids by organic extraction, yielding a medium unable to support the growth of B. burgdorferi
Summary
With an average genome of approximately 1.3 mbp [1], many aspects of cellular metabolism are minimized or absent in Borrelia burgdorferi. Such an evolutionary genome reduction is possible because B. burgdorferi lives in close association with vertebrate and tick hosts [2], which are parasitized for many common metabolites synthesized de novo by other bacteria. The acyl lipids derive from a common pathway in which glycerol-3-phosphate is twice acylated to form phosphatidic acid (PA), which is modified with choline, glycerol, or galactose [7, 8]. Precursors for all membrane constituents are presumed to be scavenged from the host as B. burgdorferi lacks apparent synthetic pathways for fatty acids, cholesterol, and choline. The membrane of in vitro–cultured B. burgdorferi appears to be mostly composed of these 4 lipid species, chromatographic fractionation
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